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Infect Immun, March 1998, p. 938-943, Vol. 66, No. 3
Departments of Medicine and Microbiology and Immunology,
Vanderbilt University School of Medicine and Veterans Affairs Medical
Center, Nashville, Tennessee1;
Laboratoire de Microbiologie A, CHU la Miletrie, 86021 Poitiers, France2;
Enteric Disease
Program, Naval Medical Research Institute, Bethesda,
Maryland3; and
Laboratory of Enteric
and Sexually Transmitted Diseases, FDA-CBER, Rockville,
Maryland4
Received 11 July 1997/Returned for modification 1 October
1997/Accepted 8 December 1997
Campylobacter jejuni is one of the leading causes of
bacterial diarrhea throughout the world. We previously found that PEB1 is a homolog of cluster 3 binding proteins of bacterial ABC
transporters and that a C. jejuni adhesin, cell-binding
factor 1 (CBF1), if not identical to, contains PEB1. A single protein
migrating at approximately 27 to 28 kDa was recognized by anti-CBF1 and
anti-PEB1. To determine the role that the operon encoding PEB1 plays in
C. jejuni adherence, peb1A, the gene encoding
PEB1, was disrupted in strain 81-176 by insertion of a kanamycin
resistance gene through homologous recombination. Inactivation of this
operon completely abolished expression of CBF1, as determined by sodium
dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and
immunoblotting. In comparison to the wild-type strain, the mutant
strain showed 50- to 100-fold less adherence to and 15-fold less
invasion of epithelial cells in culture. Mouse challenge studies showed
that the rate and duration of intestinal colonization by the mutant were significantly lower and shorter than with the wild-type strain. In
summary, PEB1 is identical to a previously identified cell-binding factor, CBF1, in C. jejuni, and the peb1A locus
plays an important role in epithelial cell interactions and in
intestinal colonization in a mouse model.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Mutation in the peb1A Locus of
Campylobacter jejuni Reduces Interactions with
Epithelial Cells and Intestinal Colonization of Mice
*
Corresponding author. Mailing address: Division of
Infectious Diseases, A-3310 Medical Center North, Vanderbilt University School of Medicine, Nashville, TN 37232. Phone: (615) 322-2035. Fax:
(615) 343-6160. E-mail:
Martin.Blaser{at}mcmail.vanderbilt.edu.
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